These changes are a result of decreased hepatic synthesis of pro- and anti-coagulation factors, thrombocytopenia, elevated von Willebrand factor (vWF), reduced a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS-13), reduced vitamin-K dependent carboxylation of pro- and anti-coagulant factors, and consumptive coagulopathy (10, 19). This evidence concerns the gene VWF and Thrombocytopenia.